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Blood, 1 March 2007, Vol. 109, No. 5, pp. 1850-1856. Prepublished online as a Blood First Edition Paper on October 24, 2006; DOI 10.1182/blood-2006-07-036046. This Article Full Text (PDF) Supplemental Methods, Tables, and Figures All Versions of this Article: blood-2006-07-036046v1 109/5/1850    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Pilotti, E. Articles by Casoli, C. Search for Related Content PubMed PubMed Citation Articles by Pilotti, E. Articles by Casoli, C. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 19, 2006 Accepted October 13, 2006 Post-genomic upregulation of CCL3L1 expression in HTLV-2 infected individuals curtails HIV-1 replication Elisabetta Pilotti, Lisa Eviri, Elisa Vicenzi, Umberto Bertazzoni, Maria Carla Re, Sonia Allibardi, Guido Poli, and Claudio Casoli* University of Parma, Italy San Raffaele Scientific Institute, Italy University of Verona, Italy University of Bologna, Italy Celbio, Italy * Corresponding author; email: claudio.casoli{at}unipr.it. Leukocytes of individuals co-infected with HTLV-2 and HIV-1 secrete chemokines that prevent CCR5-dependent (R5) HIV-1 infection of CD4+ T-cells and macrophage, with HTLV-2-induced MIP-1 as dominant HIV-1 inhibitory molecule. Two non-allelic genes code for CCL3 and CCL3L1 isoforms of MIP-1 and the population-specific copy number of CCL3L1 exerts a profound effect on HIV-1 susceptibility and disease progression. Here, we demonstrate that CCL3L1 is secreted spontaneously by leukocytes of HTLV-2 infected individuals and superinduced when cells of HTLV-2/HIV-1 multiply exposed-uninfected seronegative individuals (MEU) were stimulated with HIV-1 Env peptides. The CCL3L1 median copy number in MEU, HTLV-2/HIV-1 co-infected long-term non progressors (LTNPs) and HIV-1 mono-infected LTNPs were 1, 2, and 3, respectively. An increased CCL3L1/CCL3 mRNA ratio vs. PHA-activated healthy leukocytes was observed in both HIV-1 mono-infected LTNPs and in HTLV-2/HIV-1MEU. An additional potential correlate of HTLV-2 infection was a rapid and persistent leukocyte secretion of GM-CSF and IFN-, two cytokines endowed with CCR5 downregulation capacity. This study confirms a crucial protective role of CCL3L1 from both HIV infection and disease progression, highlighting a previously not described functional upregulation of this chemokine variant in both HIV positive and negative individuals infected with HTLV-2. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: HTLV-IIb reduces HIV infection Davide Zella Blood 2007 109: 1792. [Full Text] [PDF] This article has been cited by other articles: K. Ohba, A. Ryo, Md. Z. Dewan, M. Nishi, T. Naito, X. Qi, Y. Inagaki, Y. Nagashima, Y. Tanaka, T. Okamoto, et al. Follicular Dendritic Cells Activate HIV-1 Replication in Monocytes/Macrophages through a Juxtacrine Mechanism Mediated by P-Selectin Glycoprotein Ligand 1 J. Immunol., July 1, 2009; 183(1): 524 - 532. [Abstract] [Full Text] [PDF]

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